The heartbeat is caused by the rhythmic and orderly contraction of heart chambers surrounded by heart muscles. The normal heartbeat starts with the contraction of the atria (atrial systole) followed by contraction of the ventricles (ventricular systole) while the atria are in atrial diastole. During the following diastole, all four chambers are sequentially relaxed.
The heartbeat originates in a cardiac conduction system made up of the sinoatrial node (SA node), the internodal atrial pathways, the atrioventricular node (AV node), the Bundle of His and its various branches, and the Purkinje system. The Bundle of His conduction system spreads the heartbeat to the apex of the myocardium. The SA node typically discharges more quickly than the other portions of the system. Acting as a natural cardiac pacemaker, the SA node discharge rate generally determines the rate at which the heart beats. The impulses generated in the SA node pass through the atrial pathways to the AV node, to the Bundle of His and thence to its branches and the ventricular muscle through the Purkinje system. However, the various parts of the conduction system and the myocardium itself are capable of spontaneous discharge. The various portions of the conduction system are mostly striate, modified cardiac muscle having less than distinct boundaries.
Normally, the human heart rate is about 70 beats per second at rest. That rate is accelerated (tachycardia) by exercise, fever, and the like; the rate is slowed (brachycardia) during sleep. Other normal physical causes, e.g., breathing, cause a variation in heart rate.
There are abnormal fluctuations in the heart rate. For instance, disease may cause the so-called natural pacemaker function to shift from the SA node to the AV node. Other diseases lower the membrane potential of atrial and ventricular muscle fibers causing them to discharge repetitively. Ectopic foci of excitation of the His-Purkinje fibers result in either extrasystole (or premature beat) if the ectopic focus discharges before the expected beat or in atrial flutter (paroxysural tachycardia) if the focus repetitively discharges at a rate higher than the rate of the SA node.
These and other arrhythmias may cause benign or severe effects. Although arrythmia such as paroxysmal ventricular tachycardia are often benign, they are sometimes associated with ventricular fibrillation. Ventricular fibrillation, in which the ventricular muscle fibers contract irregularly, cause the heart to pump blood very inefficiently. The resultant serious decline in cardiac output, if untreated, is often fatal.
Control of arrhythmia is undertaken in a variety of ways. Antiarrhythmic drugs often slow conduction in the conduction system and the myocardium. Some block Na.sup.+, Ca.sup.++ channels or .beta.-adrenergic activity in the heart. These treatments are effective in clinical situations but often must be continued for extended periods of time.
Another method for controlling arrhythmia, particularly tachycardia, short of open heart surgery to surgically section the Bundle of His, is via the use of an ablation catheter. These devices are used to ablate cardiac conduction pathways.
One such device is shown in U.S. Pat. No. 4,785,815, to Cohen. Cohen shows a catheter which is inserted in typical fashion into a chamber of the heart (preferably entering the body remotely through the femoral artery) so that the distal end of the catheter may be positioned against the heart wall in close proximity to one of the cardiac conduction pathways. The catheter carries detectors for sensing various electrical potentials within the heart, e.g., the HRA (high right atrium), the HBE (His Bundle electrogram), and the VA (ventricular apex). The distal end of the catheter also carries the termination of a laser optical conduit. The laser is used to ablate the offending conduction pathway tissue. Lasering of the chosen pathway is carried out until the monitored cardiac activity is properly modified, e.g., when the Bundle of His is ablated, the surgeon notes that the atrial and ventricular activity have become asynchronous.
U.S. Pat. No. 5,056,517, to Fenici, discloses a cardiac electrocatheter optionally containing ablation wires, fiber optics, and distal and proximal electrodes for intracardial mapping.
For these and a variety of other indications, accurate mapping of cardiac electrical activity is desirable. Increasingly, the mapping of that activity is desirably more and more precise. For instance, choice of pacemaker type, proper placement of pacemaker leads, and proper programming of pacemaker variables depends in large measure upon the coronary malady to be corrected. Indeed, implantable pacemakers have been provided with an internationally adopted 4 or 5-letter code specifying which of the thousands of combinations of electrical sensing, pacing, inhibiting, etc., activities the specific pacemaker may undertake. For instance, the pacemaker chosen for a patient with acute inferior myocardial infarction is quite different from that chosen for a patient with acute anterior myocardial infarction and those likely will be quite different from pacemakers chosen for an aberrant physiological reflex such as carotid sinus hypersensitivity. In each instance, the cardiac electrical activity is different; in each case the need to properly assess the activity and then either to inhibit it or to enhance it so to restore cardiac muscle activity to a normal and proper rate is obvious to all who take the time to consider it.
Classically, electrocardiography is often undertaken noninvasively from outside the body by leads placed at specific positions on the body. Observation of the resulting signals provides preliminary information relating to cardiac electrical activity. Additional information has been achieved via use of invasive sensors such as that shown in U.S. Pat. No. 5,056,517, noted above.
None of the sensors discussed above are said to be covered with the fluoropolymeric alloy described herein.